Circular RNA Hecw1 Regulates the Inflammatory Imbalance in Spinal Cord Injury via miR-3551-3p/LRRTM1 Axis
Circular RNA Hecw1 Regulates the Inflammatory Imbalance in Spinal Cord Injury via miR-3551-3p/LRRTM1 Axis
复制标题
环状 RNA Hecw1 通过 miR-3551-3p/LRRTM1 轴调节脊髓损伤中的炎症失衡
DOI：
10.1007/s12010-022-03999-1
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发表时间：
2022-06-14
影响因子：
3
通讯作者：
Liu，Yang
中科院分区：
文献类型：
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作者：
Ban，Dexiang;Xiang，Zhenyang;Liu，Yang
脊髓损伤（Spinal cord injury，SCI）是一种神经系统疾病，具有破坏性的影响，并导致全身炎症的发展。然而，SCI的分子机制仍然没有完全阐明。本研究旨在探讨内毒素（lipopolysaccharide，LPS）对神经细胞炎症损伤的调控机制。以PC 12细胞为基础，用脂多糖建立脊髓损伤的体外模型。采用CCK-8细胞计数试剂盒测定细胞增殖情况。实时定量PCR和ELISA法检测circHecw 1、miR-3551- 3 p和炎症因子的表达。流式细胞术用于评估细胞凋亡。为了确定LRRTM 1和NF-kB信号传导的目的，进行蛋白质印迹分析。LPS诱导的PC 12细胞circ Hecw 1、TNF-α、IL-6和IL-1β的表达以及miR-3551- 3 p和IL-10的表达均显著降低。敲低circHecw 1可促进增殖，抑制凋亡，减少炎性细胞因子的表达。我们的研究表明，circHecw 1通过调节miR-3551- 3 p/LRRTM 1信号通路调节SCI神经元细胞炎症失衡。
Spinal cord injury (SCI) is a neurological disease having devastating effect and results in the development of systemic inflammation. However, the molecular mechanisms of SCI remain not entirely elucidated. This study was directed toward exploring the circ Hecw1 involved in the mechanism of lipopolysaccharide (LPS)-triggered inflammation damage in neuronal cells. The in vitro model of SCI based on PC12 cells were established with lipopolysaccharide. The cell proliferation was determined by the use of cell counting kit-8 (CCK8). The expressions of circHecw1, miR-3551-3p, and inflammatory factors were measured by quantitative real-time PCR and ELISA assay. Flow cytometry was used to assess apoptosis. Western blot analysis was performed for the purpose of determining LRRTM1 and NF-kB signaling. The expression of circ Hecw1, TNF-α, IL-6, and IL-1β in LPS-triggered PC12 cells and the expression of miR-3551-3p and IL-10 were significantly decreased. Knockdown of circHecw1 promoted proliferation and inhibited apoptosis and reduction in the inflammatory cytokine expression. Our study revealed that circHecw1 regulates SCI neuronal cell inflammation imbalance by regulating the miR-3551-3p/LRRTM1 signaling.